David DeNardo WUSM retweeted
Congratulations to Dr. Timothy Eberlein on being installed as the 107th President of @AmCollSurgeons, one of the highest honors in the surgical profession. Read more: bit.ly/3Tx3LSq

#WashUSurgery #WashUMedicine #Surgery #ACS
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David DeNardo WUSM retweeted
Submit an abstract by July 13 for the AACR Conference on Pancreatic Cancer (Sept 25-28; San Diego), chaired by Andrew J. Aguirre, Florencia McAllister, Kenneth P. Olive, Eileen O’Reilly, Diane M. Simeone, and Colin D. Weekes.
brnw.ch/21x3WSy
#AACRpan26 @EileenMOReilly
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David DeNardo WUSM retweeted
A Phase 2, Open-label Study of VS-7375, an Oral KRAS G12D (ON/OFF) Inhibitor, With & Without an Anti-EGFR Antibody, & With an Anti-EGFR Antibody & Chemotherapy, in Patients W/ Metastatic KRAS G12D-Mutated Colorectal Adenocarcinoma
(TARGET-D 203)

Phase 2 trial, 150 patients, 5 US locatio.co/paP2AFKbok

FB trial post with links to AACR25 and ASCO25 information
facebook.com/permalink.php?…
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Fine work as usual by the Lim lab. Congratulations
Drs Bansod, Lim and team. Blockade of Tumor TAK1 Induces DNA Damage and Immunogenic cGAS-STING Pathway. @SitemanCenter @WashUOncology sciencedirect.com/science/articl…
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David DeNardo WUSM retweeted
Updated RAMP205 data!

For years, drug development treated pancreatic ductal adenocarcinoma (PDAC) as a simple signaling problem awaiting the right node to inhibit. Yet PDAC behaves more like a complex adaptive system than a straight forward pathway-driven malignancy.

The inhibitors has changed that conversation. Agents like daraxonrasib are validating what was once skeptical: the driver matters more than many believed.

Yet the most interesting question may no longer be whether KRAS can be suppressed. It may be what survives after it is.

Much of the field still frames combinations through additive cytotoxicity or pathway blockade. But emerging PDAC biology suggests resistance is a property of the entire system, the adaptive ecosystem of stromal architecture, inflammatory signaling, mechanotransduction, persistence states, and host-tumor communication may be every bit as critical as the oncogenic signal itself.

This is why I view programs like RAMP-205 through a different lens. The most intriguing aspect is not the response rate alone, but the possibility that simultaneous RAF/MEK inhibition, FAK/PYK2 modulation, and chemotherapy influence multiple layers of adaptation at once. In a disease known for high attrition, this represents one of the first non-direct KRAS inhibition approaches to generate truly phenomenal early data.

The original signal was not simply an 83% ORR in a small cohort. It was the remarkable uniformity: tumor shrinkage across all evaluable patients, no progressive disease as best response, and early prolonged treatment exposure beyond historical gemcitabine/nab-paclitaxel expectations.

As the dataset expanded, the key question was whether this broader pattern, high rates of tumor shrinkage, few primary escape events, and sustained treatment delivery, would persist.
Updated data suggest elements of that signal are holding as the cohort matures.

Viewed this way, the consistency of shrinkage, encouraging durability, manageable safety, and ability to maintain therapy appear consistent with disruption of adaptive processes that let PDAC withstand pressure, a hypothesis warranting further validation.

Direct RAS inhibitors and ecosystem-directed approaches may ultimately prove complementary.

Daraxonrasib validates the driver. RAMP-205 explores the ecosystem.

The challenge ahead is not simply to inhibit the driver. It is to understand, and ultimately prevent, the mechanisms through which the system rewrites the script once the driver has been suppressed.
@Aiims1742 @VivekSubbiah @VerastemOncolog
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Enjoying watching my son do Pedal the Cause. @pedalthecause
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Congratulations Dr. Hogg and team @SciImmunology: #dendritic cells can matter in #PancreaticCancer, patients. See it at scim.ag/3UZwFHM
Big thanks to Swim Across America @SAA_Inc St. Louis and Pedal the Cause @pedalthecause for supporting this research and trial.
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David DeNardo WUSM retweeted
A dual therapy that targets conventional #dendritic cells can boost T cell-mediated antitumor immunity in #PancreaticCancer, according to a new study involving patient samples and mice. @DeNardoLabWUSM

Learn more in Science #Immunology: scim.ag/3UZwFHM
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Replying to @DeNardoLabWUSM
NIH personnel, I want you to know we as scientist appreciate all you do to support our research.
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David DeNardo WUSM retweeted
📢New human fetal pancreatic organoid model generates all three key cell types of the pancreas. New paper in @CellCellPress by @AmandaARolf , @HansClevers and collaborators. See the article here: sciencedirect.com/science/articl…
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David DeNardo WUSM retweeted
The December issue of @CD_AACR is now online! The cover features work by @olaf_klingbeil, @ChrisVakoc, and colleagues showing MARK2/MARK3 kinases are catalytic co-dependencies of YAP/TAZ in human cancer - read that, the year-in-review collection, & more: aacrjournals.org/cancerdiscover…
The December issue is online. bit.ly/41gzJE4
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David DeNardo WUSM retweeted
New #OpenAccess from @CCR_AACR
Efficacy and Safety of the Anti-IL1RAP Antibody Nadunolimab (CAN04) in Combination with Gemcitabine and Nab-Paclitaxel in Patients with Advanced/Metastatic #PancreaticCancer
aacrjournals.org/clincancerres/…
Median OS - 13.2 months
1-year survival rate - tissue IL1RAP expression
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David DeNardo WUSM retweeted
The @ChampalimaudF #PancreaticCancer symposium kicks off with an opening lecture by @EileenMOReilly @MSKCancerCenter on the oncological landscape of available & in development Rx against PDAC. A nod to KRAS targeted therapies, including freshly presented #ENA2024 data.
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David DeNardo WUSM retweeted
Dr. Lisa Coussens (@coussens_lisa) is recognized for her paradigm-shifting mechanistic studies on inflammation and cancer that identified B cell and myeloid cell significance in fostering solid tumor progression and hindering therapeutic responses: bit.ly/3A3fIFL
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Congratulations Dr. Liu @SitemanCenter and collaborators @LabBeatty and K.Bryant on their featured article in @ScienceTM . And HUDGE THANKS to @PanCAN for bringing this team together and funding the trial that came out of the science with @verastemoncology.
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Congratulations Dr. Liu and collaborators @LabBeatty and K.Bryant on their featured article in @ScienceTM. And HUDGE THANKS to @PanCAN for bringing this team together and funding the trial that came out of the science with @verastemoncology
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David DeNardo WUSM retweeted
Now online in @CD_AACR: back-to-back papers from the labs of @sastewartlab and @DeNardoLabWUSM on immunosuppression by senescent CAFs in breast and pancreatic cancers doi.org/10.1158/2159-8… doi.org/10.1158/2159-8… @jennifer_jiayu @JadBelle #DevashishSen @WUSTLmed @SitemanCenter
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Turns our MyCAFs become Senescent (SenCAFs) and can drive both breast and pancreas cancer progression through immune modulation. See just now online at Cancer Discovery
aacrjournals.org/cancerdiscover…
aacrjournals.org/cancerdiscover…
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Congratulations to Bell and Yi on back to back @CD_AACR papers. Go @sastewartlab and @SitemanCenter
aacrjournals.org/cancerdiscover…
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David DeNardo WUSM retweeted
Portrait unveiling at the conclusion of the John F DiPersio Immunotherapy Symposium
@WashUOnc @SitemanCenter @WUDeptMedicine @WUSTLmed @BarnesJewish @WUSTLdbbs @WashUDPS
#bmtsm #celltherapy #cartcells #leusm #lymsm #mmsm #mdssm
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